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PubMed1991

[Antacid therapy of upper abdominal symptoms. Double-blind study on the effect and tolerance of 2 antacids in gastritis , esophagitis and functional upper abdominal symptoms].

In a randomized, multicenter, double-blind study involving a total of 97 patients, the effectiveness and tolerance of Gelofalk, a new type of antacid combination comprising smectite--a natural alum earth, the specific molecular structure of which permits it to bind aggressive substances particularly well--aluminium hydroxide and magnesium hydroxide were investigated in comparison with a commercially available aluminium hydroxide antacid used by patients with gastritis, esophagitis and functional upper abdominal complaints over a treatment period of 4 weeks. The buffering capacity of a daily dose of Gelofalk was 135 mval, in the case of the reference antacid 210 mval. In terms of pain relief, reduction of accompanying symptoms, and endoscopic healing properties, Gelofalk proved very effective. Because of its particular properties, the preparation proved significantly superior to an aluminium hydroxide suspension in the case of most test parameters, in particular pain relief, onset of effect and heartburn. Gelofalk was very well tolerated; constipation or diarrhea occurred in only 2 cases each.

Abdominal Pain↗
PubMed1982

Intragastric and intraduodenal investigations.

This review has detailed a method for the quantification of postprandial gastric secretion and emptying based on multiple marker dilution. The method can be applied to the physiologic study of antacid therapy, allowing measurement of the effects of the antacid on gastric secretion and emptying, as well as measurement of the efficiency of antacid utilization. In our laboratory, my colleagues and I have employed this method to characterize the fate of aluminum hydroxide and magnesium hydroxide under conditions closely resembling those existing in a usual therapeutic setting. Further studies are required to compare the behavior of this class of cationic antacid with other commercial preparations and to study other factors (concomitant administration of other drugs such as H2-blockers or anticholinergics, diet, schedule, and dose) that may have an important influence on antacid utilization and their acid-neutralizing effects.

Administration, Oral↗
PubMed1986

The effect of antacids on the absorption of simultaneously ingested iron.

Most discussions of iron therapy include a statement about the ineffectiveness of iron ingested simultaneously with antacids. This study was designed to determine whether or not antacids inhibit iron absorption. A small-dose iron tolerance test was used to compare absorption of iron with and without various antacids. Liquid antacid containing aluminum hydroxide and magnesium hydroxide did not significantly decrease iron absorption. Sodium bicarbonate and calcium carbonate caused the plasma iron increase to be 50% and 67% less than the control values, respectively. However, when calcium carbonate was present in a multivitamin-plus-minerals tablet, the plasma iron change was not significantly different from control trials. Presumably the competitive binding of iron by ascorbic acid in the vitamin pill allowed uninhibited absorption of the iron. Our results suggest that certain antacids may be combined with iron therapy without reducing the efficacy of the iron.

Adult↗
PubMed1993

Effects of magnesium-aluminum hydroxide antacid on absorption of rufloxacin.

The present study was designed to determine the effects of an antacid suspension containing magnesium hydroxide and aluminum hydroxide (30 ml of Maalox) on the oral bioavailability of rufloxacin (400 mg). Rufloxacin was administered orally to 12 healthy volunteers according to a randomized, balanced, crossover design. Three treatments were administered to each subject, with a 10-day washout period between treatments; the treatments included rufloxacin alone, rufloxacin taken 5 min after antacid, and rufloxacin taken 4 h before antacid. Administration of antacid within 5 min before the administration of rufloxacin resulted in a substantial decrease in rufloxacin absorption, with a mean percent relative bioavailability compared with control values of 64% (range, 42 to 77%). Administration of antacid 4 h after the administration of rufloxacin slightly affected the absorption of the quinolone (mean relative bioavailability, 87%; range, 51 to 110%). Antacids that contain magnesium and aluminum salts reduce the absorption of rufloxacin. The extent of this interaction depends on the time that elapses between administration of the two drugs.

Administration, Oral↗
PubMed1985

In vivo and in vitro evaluation of magnesium-aluminum hydroxide antacid tablets and liquid.

The effect of magnesium-aluminum hydroxide antacid tablets or liquid on food-stimulated gastric acidity was evaluated in vivo in eight duodenal ulcer patients. Experiments were performed also in vitro. Although in vitro neutralizing capabilities of the two preparations were the same (28.3 +/- 0.1 mmol/liter), the duration of effect of tablets was longer in vivo. For example, at 3 3/4 hr after an eaten meal, mean hydrogen ion concentration with three tablets was 29.8 +/- 9.9 mmol/liter while with 15 ml liquid it was 59.6 +/- 10.3 mmol/liter (P less than 0.05). Additional studies were performed in vitro to explain the longer duration of effect of tablets compared with liquid in vivo. These experiments suggested that tablets reacted more slowly with acid than did liquid and that saliva, which was mixed with tablets during chewing, also contributed to the prolonged duration of effect.

Aluminum Hydroxide↗
PubMed1992

The effects of famotidine, ranitidine and magnesium hydroxide/aluminium hydroxide on gastric fluid pH in adult horses.

Gastric fluid pH was measured in five adult horses following nasogastric administration of famotidine, 0.5, 1.0, and 2.0 mg/kg bodyweight (bwt); ranitidine, 4.4 and 6.6 mg/kg bwt and an antacid containing magnesium hydroxide (40 mg/ml) and aluminium hydroxide (45 mg/ml), 120 and 180 ml. Fluid was aspirated through a 16 French nasogastric feeding tube at 15 min intervals, and pH was measured using a pH meter. Basal gastric fluid pH was measured at 20 min intervals for 6 h in each horse and, with the exception of two measurements of 4.66 and 4.17, ranged from 1.42 to 2.41, with a mean pH of 1.88 +/- 0.18. The response to both ranitidine and famotidine was variable between horses and between dosages. The mean gastric fluid pH values following administration of a single dose of famotidine or ranitidine were famotidine, 0.5 mg/kg bwt, 3.63 +/- 1.72; famotidine, 1.0 mg/kg bwt, 3.41 +/- 1.40; famotidine, 2.0 mg/kg bwt, 4.18 +/- 2.06; ranitidine, 4.4 mg/kg bwt, 4.07 +/- 1.25; ranitidine 6.6 mg/kg bwt, 5.34 +/- 1.12. Differences in mean gastric fluid pH between famotidine dose levels and between ranitidine dose levels were not significant (P > 0.10). Gastric fluid pH increased to greater than 6 in three horses receiving 0.5 mg/kg bwt, five horses receiving 1.0 mg/kg bwt and three horses receiving 2.0 mg/kg bwt famotidine. Gastric fluid pH increased to greater than 6 in each of the five horses receiving 6.6 mg/kg bwt ranitidine and in four of five horses receiving 4.4 mg/kg bwt ranitidine. During the 6 h post administration, ranitidine tended to increase gastric fluid pH greater than 6 longer (166 +/- 106 mins) than famotidine (98 +/- 110 mins) and this difference was nearly significant (P = 0.054). The response to antacid was variable and consistently short-lived. The mean gastric fluid pH values for 6 h after administration of 120 ml or 180 ml were 2.42 +/- 0.71 and 2.44 +/- 0.47, respectively. Gastric fluid pH increased to greater than 6 in only two horses, for 15 and 30 mins, respectively. The increase in gastric fluid pH was significantly greater for ranitidine (P < 0.001) and famotidine (P < 0.02) than for antacid. The duration of the effect was significantly longer for ranitidine doses (P < 0.001) and nearly so for famotidine doses (P < 0.055) than for antacid.

Aluminum Hydroxide↗
PubMed1996

Comparison of the effects of ranitidine effervescent tablets and magnesium hydroxide-aluminium oxide on intragastric acidity. A single-centre, randomised, open cross-over study.

In previous studies measuring intragastric pH in healthy volunteers it was shown that there was a faster onset of action with ranitidine (CAS 66357-35-5) 300 mg effervescent tablets (Zantac) compared to standard tablets. In a single-centre, randomised, open cross-over study the pH-values obtained over 6 h following the administration of one ranitidine 150 mg effervescent tablet were compared with those after aluminium oxide-magnesium hydroxide (algeldrate, CAS 1330-44-5, Al-Mg-hydroxide) 10 ml and placebo in healthy volunteers. 24 healthy male subjects between 19 and 32 years of age entered the study, 19 subjects were available for all three measurements. After an overnight fast, intragastric pH was monitored for 7 h using a glass electrode and a digital data recorder. The time in % during which the pH was > or = 3.5 and the area under the curve of the obtained pH-curves were compared. There was a highly statistically significant difference between ranitidine effervescent tablets versus Al-Mg-hydroxide and placebo whereas there was no such difference between Al-Mg-hydroxide and placebo. The onset of action of ranitidine effervescent tablets was almost immediate. It is concluded that there was a clear superiority of ranitidine effervescent tablets in healthy volunteers and it is suggested that pH-metry in patients with acidity-related diseases should be investigated for a better understanding of the function of effervescent tablets.

Adult↗
PubMed1999

Pharmacokinetics of gatifloxacin and interaction with an antacid containing aluminum and magnesium.

The pharmacokinetics of gatifloxacin (400 mg orally) and the influence of the antacid aluminum magnesium hydroxide (20 ml of Maalox 70) on the bioavailability of gatifloxacin in 24 healthy volunteers were assessed. In an open, randomized, six-period crossover study, the volunteers received either gatifloxacin alone (treatments A and D); aluminum magnesium hydroxide concomitant with gatifloxacin (treatment C); or aluminum magnesium hydroxide 2 h before (treatment B), 2 h after (treatment E), or 4 h after gatifloxacin administration (treatment F). Gatifloxacin concentrations were measured by a validated bioassay and high-performance liquid chromatography. Pharmacokinetics of a single 400-mg dose of gatifloxacin alone were characterized as follows (mean +/- standard deviation): peak concentration (Cmax), 3.8 +/- 0. 5 (treatment A) and 3.4 +/- 0.9 (treatment D) microgram/ml; time to Cmax, 1.4 +/- 0.8 (treatment A) and 1.7 +/- 0.7 (treatment D) h; area under the curve from time zero to infinity (AUC0-infinity), 33. 5 +/- 5.9 (treatment A) and 31.4 +/- 3.4 (treatment D) microgram. h/ml; urine recovery, (83 +/- 6)% (treatment A) and (84 +/- 8)% (treatment D). Comparison of the results obtained by bioassay showed a good correlation. Aluminum magnesium hydroxide administration 2 h before (treatment B) or concomitant with (treatment C) gatifloxacin decreased the Cmax by 45% (2.1 +/- 1.2 microgram/ml) or even 68% (1.2 +/- 0.4 microgram/ml) highly significantly (P < 0.01). AUC0-infinity was significantly reduced from 33.5 +/- 5.9 to 19.4 +/- 6.9 microgram. h/ml (by 42%) or even to 11.9 +/- 3.3 microgram. h/ml (by 64%) (P < 0. 01). If aluminum magnesium hydroxide was given 2 h after gatifloxacin (treatment E), there was no significant reduction of concentration in serum but AUC0-infinity was significantly reduced from 31.4 +/- 3.4 to 25.9 +/- 5.3 microgram. h/ml (18%) (P < 0.01). Aluminum magnesium hydroxide given 4 h after gatifloxacin (treatment F) showed no influence on the gatifloxacin pharmacokinetics. Therefore, the optimal time between gatifloxacin application and the intake of an aluminum-containing antacid should be 4 h.

Administration, Oral↗
PubMed1978

Impaired absorption of desmethyldiazepam from clorazepate by magnesium aluminum hydroxide.

Ten healthy volunteers ingested single 15-mg doses of clorazepate dipotassium (CZP) with 60 ml of water, or with 60 ml of magnesium aluminum hydroxide (Maalox), on two occasions in a randomized, two-way crossover study. Plasma concentrations of desmethyldiazepam (DMDZ) were determined in multiple samples drawn during 48 hr after each dose. Mean kinetic variables for DMDZ in CZP-water and CZP-magnesium aluminum hydroxide treatment conditions, respectively, were: peak measured concentration, 273 and 188 ng/ml (p 0.001); time of peak concentration, 1.8 and 2.8 hr after dose (p less than 0.01); apparent absorption half-life, 14.8 and 30.7 min (p less than 0.02); area under the 48-hr plasma concentration curve, 6,028 and 5,433 ng/ml X hr (p less than 0.02). Self-rated sensations of feedling "spacey," "thinking slowed down," and of generalized sedation, were reported with both treatment conditions, but these subjective effects occurred earlier and were more profound when CZP was taken with water as opposed to magnesium aluminum hydroxide. Thus administration of single doses of CZP with usual doses of a commonly prescribed antacid reduces the rate and extent of appearance in blood of DMDZ (the compound responsible for clinical activity) and attenuates self-rated clinical effects.

Adult↗
PubMed1996

Effect of aluminum hydroxide/magnesium hydroxide antacid and bismuth subsalicylate on gastric pH in horses.

OBJECTIVE: To assess the effect of aluminum hydroxide/magnesium hydroxide antacid and bismuth subsalicylate on gastric pH in clinically normal horses and to develop guidelines on the use of these agents for treatment of peptic ulcer disease in horses. DESIGN: Prospective, randomized, controlled trial. ANIMALS: 5 clinically normal adult horses with chronically implanted gastric cannulas. PROCEDURE: Each horse received all 5 treatments (30 g of aluminum hydroxide/15 g of magnesium hydroxide, 12 g of aluminum hydroxide/6 g of magnesium hydroxide, 10.5 g of bismuth subsalicylate, 26.25 g of bismuth subsalicylate, and 5% methylcellulose control) with only 1 experiment performed each day. Gastric pH was measured via a glass electrode inserted through the gastric cannula for 1 hour before treatment and continued for 2 hours after treatment. Food or water was not given to the horses during the experiment. Measurements of gastric pH obtained during posttreatment hours were compared with pretreatment gastric pH values. RESULTS: Only a dose of 30 g of aluminum hydroxide/ 15 g of magnesium hydroxide resulted in a significant increase in gastric pH over baseline or control values. Mean pH was 5.2 +/- 0.62 and 4.59 +/- 0.48 for posttreatment hours 1 and 2, respectively. CLINICAL IMPLICATIONS: Oral administration of 30 g of aluminum hydroxide/15 g of magnesium hydroxide to adult horses should result in a mean hourly gastric pH > or = 4.0 for at least 2 hours.

Administration, Oral↗
PubMed1990

Effects of magnesium-aluminum hydroxide and calcium carbonate antacids on bioavailability of ofloxacin.

The effects of 15- and 5-ml doses of magnesium-aluminum hydroxide (MAH) and calcium carbonate (CC) antacids, respectively, on the bioavailability of ofloxacin after single oral 400-mg doses of ofloxacin were investigated in a 32-subject, randomized, crossover, open-label study. On four separate occasions, subjects received ofloxacin alone or antacid 24 h before, 2 h before, or 2 h after ofloxacin administration (n = 16 for each antacid). CC administration had no significant effect on the rate and extent of ofloxacin absorption regardless of the timing of antacid administration. A small but significant negative effect of MAH administration 2 h before ofloxacin administration was noted as evidenced by area under the curve and peak concentration in plasma data. Simultaneous administration of ofloxacin with either antacid was not investigated in this study. It appears that MAH and CC antacids in the doses used in this study generally do not interfere in a clinically significant manner with the bioavailability of ofloxacin, provided that an interval of at least 2 h separates the administration of these products.

Adolescent↗
PubMed1987

The carry-over effect on the bowel habit in elderly long-term patients of long-term bulk-forming products containing stimulant laxative.

This study was undertaken to investigate the possible carry-over effect on elderly long-term patients of bulk-forming products containing stimulant type laxatives. Thirty-six patients received magnesium hydroxide daily for a mean period of 10 months prior to the study, and 23 patients received bulk laxatives containing cassiae senna daily for a mean period of 13 months prior to the study. The pre-study laxatives were randomly changed either to magnesium hydroxide or to bulk laxatives. In the patient group receiving a bulk-forming product containing stimulant type laxative long-term prior to the study, the need for additional stimulant laxatives during the pure bulk laxative (3.0 vs. 3.8/4 weeks, NS) or magnesium hydroxide treatment (2.6 vs. 2.7/4 weeks, NS) was not more frequent and the frequency of defaecation was not lower than in the patients (during bulk laxative 11.2 vs. 9.3/4 weeks, NS and during magnesium hydroxide 12.0 vs. 13.7/4 weeks, NS) who received long-term magnesium hydroxide treatment prior to the study. Thus, our data indicated no carry-over effect after the use of bulk-forming laxatives containing senna for 13 months in elderly long-term patients.

Aged↗
PubMed1983

Interaction of antacids with antiarrhythmics. V. Effect of aluminium hydroxide and magnesium oxide on the bioavailability of quinidine, procainamide and propranolol in dogs.

The influence of aluminium hydroxide and magnesium oxide on the oral bioavailability of quinidine, procainamide and propranolol in the dog was investigated. The administration of aluminium hydroxide with a quinidine sulfate capsule causes a significant decrease of maximal plasma concentration (Cpmax) and a shift in tmax (time to reach Cpmax). The area under the curve is not significantly decreased. Administration of magnesium oxide together with a quinidine sulfate capsule or a sustained-release preparation of quinidine bisulfate causes a significant decrease of both Cpmax and the area under the curve. A shift of tmax was observed for the conventional preparation only. The administration of aluminium hydroxide with procainamide hydrochloride diminishes only Cpmax in a significant way. Administration of magnesium oxide together with procainamide hydrochloride has no influence on the different parameters. Administration of aluminium hydroxide or magnesium oxide with propranolol hydrochloride has a significant negative influence on both the Cpmax and the area under the curve.

Aluminum Hydroxide↗
PubMed1992

Norfloxacin interaction with antacids and minerals.

The urinary excretion of norfloxacin was measured in eight healthy volunteers after its co-administration with a variety of over-the-counter preparations, each containing a different metal ion. Commonly used doses of ferrous sulphate, zinc sulphate, aluminium hydroxide and magnesium hydroxide reduced the 24 h urinary excretion of norfloxacin by 50 to 90%. Bismuth subsalicylate had no significant effect. In vitro experiments demonstrated the formation of complexes between norfloxacin and iron, zinc, aluminium, and magnesium ions, respectively. Many pharmaceuticals contain the same metal ions that caused significant interactions with norfloxacin. The efficacy of norfloxacin treatment may be compromised when it is taken concurrently with preparations containing these metal ions.

Adult↗
PubMed1983

Metabolic alkalosis due to absorption of "nonabsorbable" antacids.

In a patient with end-stage renal disease undergoing long-term maintenance hemodialysis, moderately severe metabolic alkalosis developed in the absence of vomiting or gastric drainage. The cause of the acid-base disorder was exogenous alkali administration, in the form of combined ingestion of "nonabsorbable" antacids (aluminum hydroxide and magnesium hydroxide), neutral phosphate, and a cation-exchange resin (sodium polystyrene sulfonate). In this report, the relevant data of this patient are detailed, and the literature on this well-documented, albeit poorly recognized, acid-base derangement is summarized.

Absorption↗
PubMed1995

The role of intragastric acidity and stress ulcus prophylaxis on colonization and infection in mechanically ventilated ICU patients. A stratified, randomized, double-blind study of sucralfate versus antacids.

UNLABELLED: This study evaluates the effects of sucralfate and antacids on intragastric acidity, colonization of stomach, oropharynx and trachea, and the incidence of ventilator-associated pneumonia (VAP) in mechanically ventilated patients in intensive care units. We conducted a prospective randomized double-blind trial in which patients were stratified on initial gastric pH. Intragastric acidity was measured with computerized, continuous intragastric monitoring. The diagnosis of VAP was established with protected specimen brush and/or bronchoalveolar lavage. The study included consecutive eligible patients with mechanical ventilation and nasogastric tube. INTERVENTIONS: After stratification on initial intragastric pH into two groups, patients from both groups were randomly assigned to receive either antacids (a suspension of aluminum hydroxide and magnesium hydroxide), 30 mL every 4 h, or sucralfate, 1 g every 4 h. Continuous intragastric pH monitoring was performed in 112 patients (58 antacids, 54 sucralfate). Using predetermined criteria, colonization of stomach, oropharynx, and trachea, and the incidence of VAP were assessed. Altogether, 141 patients were included (74 receiving antacids, 67 sucralfate) and continuous intragastric pH monitoring was performed in 112 patients, with a mean of 75 h per patient. The median pH and the percentage of time with a pH < 4.0 were calculated from each measurement. No significant differences in median pH values (4.7 +/- 2.2 and 4.5 +/- 2.0 for antacids and sucralfate, respectively) were observed. Median pH values were higher in patients with gastric bacterial colonization than in noncolonized patients (5.5 +/- 2.1 and 3.3 +/- 2.0, p < 0.01), but colonization of oropharynx and trachea was not related to intragastric acidity. Thirty-one patients (22%) developed VAP, with a similar incidence in both treatment groups. In addition, antibiotic use, duration of hospitalization, and mortality rates were similar in both groups. Enteral feeding did not change intragastric acidity significantly but increased gastric colonization with Enterobacteriaceae, without influencing oropharyngeal and tracheal colonization. Antacids and sucralfate had a similar effect on intragastric acidity, colonization rates, and incidence of VAP. Intragastric acidity influenced gastric colonization but not colonization of the upper respiratory tract or the incidence of VAP. Therefore, it is unlikely that the gastropulmonary route is important for the development of VAP.

Antacids↗
PubMed1994

Nosocomial pneumonia in mechanically ventilated patients receiving antacid, ranitidine, or sucralfate as prophylaxis for stress ulcer. A randomized controlled trial.

OBJECTIVE: To assess three anti-stress ulcer prophylaxis regimens in mechanically ventilated patients for bacterial colonization, early- and late-onset nosocomial pneumonia, and gastrointestinal bleeding. DESIGN: Randomized controlled trial. PATIENTS: Consecutive eligible patients with mechanical ventilation and a nasogastric tube. Of 258 eligible patients, 244 were assessable. SETTING: Medical and surgical intensive care units. INTERVENTION: At intubation, patients were randomly assigned to receive one of the following: antacid (a suspension of aluminum hydroxide and magnesium hydroxide), 20 mL every 2 hours; ranitidine, 150 mg as a continuous intravenous infusion; or sucralfate, 1 g every 4 hours. MEASUREMENTS: Using predetermined criteria, the incidence of gastric bleeding, gastric colonization, early-onset pneumonia, and late-onset pneumonia was assessed in patients intubated for more than 24 hours. RESULTS: Of 244 assessable patients, macroscopic gastric bleeding was observed in 10%, 4%, and 6% of patients assigned to receive sucralfate, antacid, and ranitidine, respectively (P > 0.2). The incidence of early-onset pneumonia was not statistically different among the three treatment groups (P > 0.2). Among the 213 patients observed for more than 4 days, late-onset pneumonia was observed in 5% of the patients who received sucralfate compared with 16% and 21% of the patients who received antacid or ranitidine, respectively (P = 0.022). Mortality was not statistically different among the three treatment groups. Patients who received sucralfate had a lower median gastric pH (P < 0.001) and less frequent gastric colonization compared with the other groups (P = 0.015). Using molecular typing, 84% of the patients with late-onset gram-negative bacillary pneumonia were found to have gastric colonization with the same bacteria before pneumonia developed. CONCLUSION: Stress ulcer prophylaxis with sucralfate reduces the risk for late-onset pneumonia in ventilated patients compared with antacid or ranitidine.

Adult↗
PubMedDate not supplied

Low-dose antacids versus ranitidine in the short-term treatment of patients with duodenal ulcer. Endoscopic and histologic placebo-controlled study.

In this double-blind randomized placebo-controlled trial we compared the efficiency of two Polish antacids (Alugastrin, dihydroxyaluminium sodium carbonate and Alumag, aluminium hydroxide with magnesium hydroxide; buffering capacity 189 and 224 mmol) with ranitidine in the healing of duodenal ulcer. We also examined the effect of drugs on the frequency and severity of gastritis and selected morphometric parameters of the fundic mucosa. The study showed that low-dose antacids effectively promote the healing of duodenal ulcer during four week therapy, similarly to ranitidine (72%, 76% and 80%, respectively) and significantly better than placebo (46%). Both antacids and ranitidine were without effects on the chronic gastritis and did not cause any trophic changes of the gastric mucosa.

Adult↗